This invention relates to a method of treatment to reduce or eliminate the symptoms of smoking withdrawal syndrome in tobacco smokers and thereby make it easier for them to stop smoking.
Known methods of treating tobacco addiction have met with limited success. Anti-smoking clinics using a variety of methods report a long term success rate of from 10% to 20% (Higenbottom T. and Chamberlain A. (1984) Thorax, 39, 641-646).
To date no attempt to treat tobacco addiction by a clinical approach based on an understanding of the physiological effects of nicotine has been reported.
The immediate physiological effect of nicotine inhalation is a temporary rise in blood sugar which produces the `lift` experienced by smokers (Haggard H. and Greenberg L. (1934) Sience, 79, 165-166). This rise in blood sugar is the result of an increased output of glucocorticoids by the adrenal cortex in response to stimulation by endogenous corticotrophin secreted by the anterior pituitary gland in response to unphysiological stimulation with nicotine (Kershbaum A. et al. (1968) J.A.M.A., 203, 275-278). It therefore appears that the lift associated with smoking is initiated by the secretion of corticotrophin.
It is possible that in smokers the capacity of the anterior pituitary gland to produce normal quantities of corticotrophin is impaired by repeated unphysiological stimulation with nicotine. This would result in secondary hypoadrenocorticism and a consequent reduced output of glucocorticoids with a tendency to hypoglycaemia. The later would result in a reflex increase in adrenaline production which would tend to simultaneously correct the hypoglycaemia and cause feelings of nervous tension. The hunger caused by the low blood sugar and the nervous tension caused by the extra circulating adrenaline may be the basis of smoking withdrawal syndrome. Relief of these symptoms by nicotine inhalation is believed to be the result of nicotine-stimulated secretion of endogenous corticotrophin.